HIV

1. HIV INFECTIONS
DR.YASHWANT INGLE
1ST YEAR P.G.

2. HIV INFECTIONS
 Disease :Acquired immune deficiency
syndrome.
 First recognized in 1981.
 Caused by Human Immunodeficiency Virus
(HIV-1).
 Unpleasant and fatal disease.
 AIDS the terminal phase of HIV infection

3. EPIDEMIOLOGY
 Since 1981 AIDS has grown to be the
second leading cause of disease burden
worldwide and leading cause of death.
 In 2000, WHO estimated there were over 36
million people living with HIV/AIDS.
 In India it is estimated that 4 million
persons are infected.

4. The Normal immune System
 Protects the body
 Consists of lymphoid organs and tissues
 All of its components are vital in the production and
development of lymphocytes
 B-cells and T-cells are produced from stem cells in
the bone marrow
 B-cells recognize specific antigen targets and secrete
specific antibodies

5. T-cells regulate the immune system and kill cells that
bear specific target antigens
 CD4+ cells are helper cells that activate B-cells, CD8
and macrophages when a specific antigen is present
 Phagocytes include monocytes and macrophages
 The complement system consists of 25 proteins
 When the immune system is weakened or destroyed by
a virus such as HIV, the body is vulnerable to
opportunistic infections (OIs)

6. Human Immunodeficiency Virus
HIV is a retrovirus that uses
its RNA and the host’s DNA
to make viral DNA. It has a
long incubation period.
 HIV consists of a
cylindrical center
surrounded by a sphere-
shaped lipid envelope.
The center consists of
two single strands of
RNA.
 HIV causes severe damage
to and eventually destroys
the immune system by
utilizing the DNA of CD4+
lymphocytes to replicate
itself, destroying the CD4+
lymphocyte.

7. HIV Lifecycle
 Host cells infected with HIV have a very short lifespan.
 HIV continuously uses new host cells to replicate itself.
 Up to 10 million individual viruses are produced daily.
 During the first 24 hours after exposure, the virus
attacks or is captured by dendritic cells (type of
phagocyte) in mucous membranes and skin.
 Within five days of exposure, infected cells make their
way to lymph nodes and then to the peripheral blood,
where viral replication becomes very rapid.

8. Phases: binding and entry, reverse transcription,
replication, budding, and maturation

9. The Chronology of HIV-Induced Disease
1. Primary HIV Infection and Seroconversion
 Clinical features
 Seroconversion illnesses
2. Stages of Disease Progression
 Early immune depletion
 Intermediate immune depletion

10. Primary HIV Infection
and Seroconversion
Clinical Features
 On first exposure, there is a 2-4 week period of
intense viral replication before the onset of an immune
response and clinical illness.
 Acute illness lasts from 1-2 weeks and occurs in 53%
to 93% of cases.
 Clinical manifestations resolve as antibodies to the
virus become detectable in patient serum.
 Patients then enter a stage of asymptomatic infection
lasting months to years.

11. Seroconversion Illness
 Manifests as a flu-like syndrome: fever, myalgia, etc.
 Neurological symptoms: HIV in CSF, aseptic
meningoencephalitis, etc.
 Gastrointestinal symptoms: mucocutaneous ulceration,
pharyngeal edema, etc.
 Dermatological symptoms: rash, urticaria, etc.

12.  Laboratory Findings
 First 1-2 weeks:
 Profound reduction in CD4, CD8 lymphocyte
counts
 Peripheral lymphocytosis
 Mild thombocytopenia
 First 2-6 weeks:
 Antibodies to HIV detected
 HIV antigen may be detected in serum
before antibodies

13.  Management
• Clinical management is primarily symptomatic
• Goal is to give appropriate counseling and
education to prevent further spread
• Issues to consider:
 Tentative nature of diagnosis
 Patient’s self-reproach
 Implication for patient’s lifestyle
 Contact tracing to identify source

14. Stages of Disease Progression
 Early Immune Depletion (CD4 cell count > 500/mL)
• During this stage, level of virus in blood is very
low
• HIV replication taking place mostly within lymph
nodes
• Generally lasts for five years or more
• Persistent Generalized Lymphadenopathy (PGL)
without other symptoms may be noted
• Usually symptom-free, but several autoimmune
disorders may appear

15. Stages of
Disease Progression, continued
 Intermediate Immune Depletion
(CD4 cell count between 500 and 200/ mL)
• Immune deficiency increases
• Infections commence and persist or increase as the
CD4 cell count drops
• Consider commencing first-line ARV therapy
• Consider preventive treatment for TB and
Cotrimoxazole PT
• Less severe infections, particularly of skin and
mucosal surfaces, appear
• Other infections begin to manifest

16. Stages of
Disease Progression, continued
 Advanced Immune Depletion (CD4 cell <200/ mL)
Case definition of AIDS is having a CD4 cell
count of less than 200/ mL

17. TRANSMISSION
OF HIV
INOCULATION OF BLOOD
 Transfusion of blood and blood products
 Needle sharing in iv drug abusers.
 Needle stick accidcents.
 Open wounds or mucous membrane
exposure in health care workers.

18. SEXUAL TRANSMISSION
 Male homosexuals.
 Heterosexual contacts
 Prostitution.
 Unprotected sex.
PERINATAL
 Intrauterine
 Peripartum
 Breast milk.

19. HIGH RISK GROUPS
 Homosexuals
 Professional blood donors.
 Drug abusers.
 Prostitutes.
 Haemophillics.
 Infants of sexually promiscuous mothers.
 Unprotected sex.

20. WHAT CAUSES AIDS
 Transmission is usually through infection
with blood, semen,vaginal fluid containing
HIV-1 or the related HIV-2.

21. HIV-1
 HIV-1 was first introduced in humans in
1930s.
 Virus originated from closely related
African primate virus, simian
immunodeficiency virus.
 Immune deficiency is a consequence of
high level continuous HIV replication.

22. HIV VIRUS

23. VIRUS STRUCTURE
 The retro virus comprises a single taxonomic
group of RNA viruses.
 Eacxh viral particle is about 100nm in
diameter.
 They contain enzyme reverse transcriptase
which is a RNA dependent DNA polymerase.
 These have an envelope composed of lipid and
viral proteins.

24. VIRAL REPLICATION
 Retro viruses are different from other
viruses since they replicate and produce
viralRNA from a DNA copy of the virion
RNA, through the action of reverse
transcriptase.

25. HIV Uncoating
Genome RNA
Reverse trans
DNA copy
Cellular DNA
Integrase
HIV genomic RNA
Translation
Peptide chains
Viral proteins
Protease
Assembly
Release

26. VIRAL REPLICATION

27. HIV-1 envelope glycoprotein gp 120 binds
specifically to CD4 molecule of T- helper
lymphocytes.
Virus enters the host cell by membrane
fusion and RNA is released.
Under the influence of reverse transcriptase a
doble stranded copy of DNA is produced
DNA is cicularised, passes into nucleus and is
spliced into host cell DNA as provirus.

28. HERE THE INFECTION STARTS
Host RNA polymerase transcribes mRNA from the
provirus to produce viral mRNA.
New virions are assembled at the cell membrane
where envelope and core proteins are located.
Virion released by budding
PRODUCTIVE GROWTH CYCLE
HOST CELL IS DESTROYED

29. SIGNS AND SYMPTOMS
 Initial exposure (sero conversion)
Flu like symptoms Fever
Weakness
 Asymptomatic stage
Serological evidence of infection
 Symptomatic stage
T4/T8 ratio reduced to 1.
Oral candidosis
Night sweats
Diarrhea
Weight loss
Persistent lymphadenopathy.

30.  Advanced symptomatic stage
 Serological evidence of infection.
 T4/T8 ratio suppressed to less than 1.
 HIV encephalopathy.
 HIV wasting syndrome.
 Major oppurtunistic infections.
 Neoplasms Kaposi’s sarcoma
Lymphoma
Carcinoma of rectum

31. LAB DIAGNOSIS
 A specific virological diagnosis of HIV infection
can be achieved in several ways.
 Current lab tests depends on antibody detection.
 An Enzyme Linked Immuno Sorbent Assay
(ELISA) test is initially performed for the
detection of HIV antibody.
 Positive results are confirmed further by
examining further blood samples using formats
such as Radioimmuno assay or
immunofluoresence.

32. LAB DIAGNOSIS
 Serology
Demonstration of specific anti HIV
antibodies.
Mainstay of clinical diagnosis
 Viral culture
Slow process
Not routinely available

33.  Viral antigen (p24)
Present briefly at the time of infection.
Reappears late in infection.
Correlates with the degree of viraemia.
Not available routinely.
 Viral nucleic acid
Polymerase chain reaction with
intermediate serological results.
May have role in confirming infection in
babies born to carrier mothers.

34. ECC CLEARINGHOUSE
CRITERIA 1993

35. Revised classification
 combined necrotizing ulcerative gingivitis
and necrotizing ulcerative periodontitis
 oral squamous cell carcinoma has been
added
 In the category of Salivary Gland Disease’,
salivary gland enlargement and salivary
hypofunction are considered as two separate
conditions

37. ORAL MANIFESTATIONS
OF HIV
 FUNGAL INFECTIONS
Candidosis Pseudo membranous
Erythematous
Hypoplastic
Angular chelitis
Histoplasmosis
Cryptococcosis
Geotrichosis

38.  BACTERIAL
Linear gingival erythema.
Necrotising ulcerative gingivitis.
Necrotising stomstitis.
Actinomycosis
 NEOPLASMS
Kaposi’s srcoma
Non hodgkins lymphoma.

39.  VIRAL
Herpes simplex
Herpes zoster
Cyto megalo virus
Human papilloma virus oral warts
condyloma
Ebstein barr virus hairy leukoplakia

40.  OTHERS
Facial palsy
Trigeminal neuropathy
Recurrent apthous ulceration
Immune thrombocytopenic purpura
Xerostomia
Salivary gland enlargement
Melonotic pigmentation.

41. CANDIDIASIS
 Many times candidal infection can be first
sign or symptom of HIV infection.
 May cause discomfort or pain or halitosis.
 Signals decline of immune function.
 Eosophageal candidiasis is an AIDS
defining diagnosis.

42. CANDIDIASIS
Agular chelitis
Angular chelitis
and hyperplastic
candidiasis of
tongue.

43. CANDIDIASIS
Pseudomembranous Florid candidiasis

44. CANDIDIASIS
Erythematous
candidiasis
Atrophic candidiasis

45. CANDIDIASIS
 TREATMENT
 Nystatin
 Clotrimazole 100 mg OD
 Mycelex
 Ketocanazole 200-400 mg OD
 Fluonazole 100 mg OD
 .12% Chlorhexidine
 Pilocarpine 5mg TDS

46. HISTOPLASMOSIS
Histoplasmosis capsulatun infection

47. HISTOPLASMOSIS
 Caused by histoplasma capsulatum.
 Oppurtunistic infection.
 TREATMENT
Amphotericin B

48. HSV-1
Herpetic whitlow Herpes labialis

49. HSV-1
 Attacks of Herpes Simplex are more severe
in AIDS patients
 Lesions involve skin and oral mucosa.
 Intra oral recurrent Herpes can occur on any
mucosal surface.
 TREATMENT
 Acyclovir 1-1.4 mg for 7-10 days

50. ORAL HAIRY LEUKOPLAKIA
Limited hairy
leukoplakia
Extensive hairy
leukoplakia

51. ORAL HAIRY LEUKOPLAKIA
 OHL is caused by epstein barr virus.
 Almost allways present.
 Mainly on lateral borders of tongue.
 Can occus on any mucosal surface.
 Mainly in homosexuals and bisexual men.
TREATMENT
Acyclovir 2-3g orally OD for 2 weeks.

52. VARICELLA VIRUS
Reactivation of latent
varicella virus
Shingles

53. VARICELLA VIRUS
 Risk of reactivation of latent virus.
 Vesicles are formed.
 Unilateral pattern.
 Pain and pruritis is associated.
 TREATMENT
Acyclovir 800 mg 5/day for 7-10 days.

54. HUMAN PAPILLOMAVIRUS
A large veneral wart Veneral wart on tongue

55. HUMAN PAPILLOMAVIRUS
 There is an increase of some strains of HPV
in HIV infected patients.
 Genital and anal condylomata.
 Oral condylomas.
 TREATMENT
Lasers
Cryosurgery
Electrosurgery

56. LINEAR GINGIVAL
ERYTHEMA

57. LINEAR GINGIVAL
ERYTHEMA
 Persistent linear, easily bleeding,
erythematous gingivitis.
 Localized or generalized in nature.
TREATMENT
 Unresponsive to any kind of treatment.

58. NECROTISING ULCERATIVE
GINGIVITIS
Severe gingival
clefting
Progressive gingival
recession

59. NECROTISING ULCERATIVE
PERIODONTITIS

60. NECROTISING ULCERATIVE
PERIODONTITIS
 Rapidly progressing.
 Bone loss and attachment loss.
 Soft tissue necrosis.
 Rapid periodontal destruction.

61. KAPOSI’S SARCOMA
Kaposi’s sarcoma of the skin. KS involving cervical
lymph node

62. KAPOSI’S SARCOMA
Nodular KS Advanced nodular
KS

63. KAPOSI’S SARCOMA
KS involving tongue. KS involving palate.

64. KAPOSI’S SARCOMA
 Malignant reactive lesion.
 Occurs in all AIDS groups.
 More in homosexuals and bisexual males.
 HIV infected are 7000 folds more likely to
develop KS.
 KS is malignant and grows slowly but in AIDS it
spreads rapidly.
 Skin most common site.
 Initially flat red purple arythemetic lesion.
 Later in the course take nodular painful form.

65. NON HODGKIN’S
LYMPHOMA

66. DRUGS OF SIGNIFICANCE
TO THE DENTIST
 ANTIBIOTICS
Erythromycin
Clarithromycin
Streptomycin
Clindamycin
Azithromycin
Metronidazole
Ethambutol

67.  ANTIFUNGALS
Nystatin
Ketocanazole
Clotrimazole
Amphoterin B
 ANTIVIRALS
Acyclovir
Valacyclovir

68. PREVENTION
 Risk reduction.
 Public education programes.
 Distribution of free sterile needles.
 Use of condoms.
 Use of protective work wear.
 Avoid needle stick accidents.

69. CROSS INFECTION
 The evidence of the transmission of HIV is
fragmentary.
 Unless gross blood contamination or needle
stick injury occurs, then HIV is unlikely to
cause infections in dentistry.
 Many dentist have simply reacted by stating
that they would refuse to treat HIV infected
patient.

70. CROSS INFECTION
CONTROL
 Cross infection control is the sum total of all
the measures taken to prevent subsequent
infection.
 By using certain infection control measures
HIV infected patients can be treated by
general dental practitioners.

71. IDEAL CROSS INFECTION
PROCEDURES
 Simple
 Easily reproduced.
 Economical.
 Easily understood.
 Should not involve toxic substances.

72. IDENTIFICATION OF PATIENT
AT RISK
 Routine use of the medical history has been
advocated as the method of identification of
HIV infected patient.
 Situation is complex as questions
concerning sexual proclivities are difficult
and often embarasing to ask.
 But history of the patient may help for the
provisional diagnosis of AIDS.

73. CROSS INFECTION
CONTROL
1. IDENTIFICATION OF PATIENT AT
RISK.
2. HAND CARE.
3. EYE CARE.
4. MASKS.
5. NEEDLE STICK INJURY.

74. PREVENTIVE MEASURES
HAND CARE
 Any noticable injury
should be covered
protective water proof
adhesive dressing.
 Double gloves canbe
used.
MASKS
 Theatre type well
fitting masks can be
used.
 Prevents direc spread
of droplets from the
operator on to the
patient.

75. EYE CARE
 Non corrective or
corrective eye wear.
 Well fitting glasses
which cover the eyes
properly can be used.
 Comfertable side
pieces will add on the
protection.

76. NEEDLE STICK
INJURY
 Serious form of occupational injury.
 Injuries in which contaminated material is
introduced by a sharp object through
epithelium.

77. NEEDLE STICK INJURY
Wash in running water
Encourage wound to bleed
Cover the wound
Consider referral to medical practitionar.
Prophylactic
Hyperimmuno gammaglobulin
Azothymidine

78. THANK YOU